Dilated cardiomyopathy is characterized by an enlarged, thin walled, poorly functioning heart. While this condition can be caused by a multiplicity of factors, one recognized etiology is chronic tachycardia. The goals of this project are: (1) identify the cellular and extracellular alterations responsible for the ventricular dilatation and dysfunction with developing cardiomyopathy, (2) quantify the residual ventricular dysfunction and abnormal geometry during the regression of dilated cardiomyopathy, and (3) examine the cellular and extracellular mechanisms potentially responsible for these permanent alterations. The applicant would perform a longitudal study using a pacing induced model of cardiomyopathy and recovery to: (a) measure the systolic and diastolic properties of the ventricular chamber, (b) compute changes in myocyte geometry, ultrastructural composition, function, and adhesion capacity, and (c) examine collagen content, type, distribution, geometric conformation, and gene expression of collagen types within the ventricular wall. In this way, the structural and functional changes to the ventricle could be directly related to cellular and extracellular events.